C linical F ocus : H ospital A dmissions , L atest P rotocols , P erioperative M edicine , and T ransitions of C are
Summary of Clinical Practice Guidelines for Acute Kidney Injury
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DOI: 10.3810/hp.2014.02.1086
Carl P. Walther, MD 1 Amber S. Podoll, MD, FACP 1 Kevin W. Finkel, MD, FACP, FASN, FCCM 1 1 University of Texas Health Science Center at Houston, Department of Medicine, Division of Renal Diseases and Hypertension, Houston, TX
Abstract: Clinical practice guidelines are intended to standardize the diagnosis and treatment of diseases in order to improve both patient outcomes and resource utilization, using evidence-based criteria. As recently as a decade ago, there was no agreed upon definition of acute kidney injury (AKI), making it difficult to conduct proper clinical studies on the epidemiology and treatment of the disorder. Following the advent of the Risk, Injury, Failure, Loss, and End-stage (RIFLE) criteria for defining AKI, several guidelines for the diagnosis and management of AKI have been developed. In our review, we present a narrative description and comparison of the major published guidelines. Overall, there has been significant agreement among the various guidelines, and each seems well-reasoned and clinically useful. Perhaps the most striking conclusion upon review of the various guidelines is the limited scope of knowledge about optimal management of patients with AKI. Keywords: acute kidney injury; practice guidelines; evidence-based medicine; clinical trials
Introduction
Correspondence: Kevin W. Finkel, MD, FACP, FASN, FCCM, Professor and Director, Division of Renal Diseases and Hypertension, UT Health Science Center at Houston, 6431 Fannin, Houston, TX 77030. Tel: 713-500-6868 Fax: 713-500-6882 E-mail: [email protected]
Acute kidney injury (AKI) is common among hospitalized patients, and is associated with significant morbidity and mortality.1,2 Despite increasing recognition of its associated medical consequences, there remains significant uncertainty regarding optimal management of patients with AKI. Initially, lack of a consistent definition of AKI limited efforts to conduct proper clinical trials and improve patient outcomes. H owever, in recent years, consensus definitions have been developed and widely adopted (Table 1). Most management strategies for AKI are best described as “supportive care,” and rarely is established AKI remediable through specific interventions.3–5 Renal replacement therapy (often referred to as “renal support” in recognition of the inability to fully replace kidney function), is an active area of research because issues such as timing, modality, and dose remain controversial.6,7 Similarly, several questions remain regarding prevention and management of AKI, including adequacy of volume resuscitation, type of resuscitation fluid (colloid versus crystalloid), and use of various pharmacologic agents (n-acetyl-cysteine, sodium bicarbonate, dopamine agonists, and natriuretic peptides). Therefore, there is a great need for clinical practice guidelines in the field of AKI.
Materials and Methods
Published guidelines on the diagnosis and management of AKI were located through an electronic search of PubMed, Cochrane Reviews, and medical society web pages. The 2010 American Thoracic Society (ATS) guideline,8 the 2011 Renal Association United Kingdom (UK) guideline,9 the 2012 Kidney Disease Improving Global Outcomes (KDIGO) guideline,10 and a draft released in 2013 of proposed National Institute for
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Table 1. AKI Staging Context
RIFLE-Risk AKIN/KDIGO-1
RIFLE-Injury AKIN/KDIGO-3
RIFLE-Failure AKIN/KDIGO-3
RIFLE-Loss
RIFLE-ESRD
RIFLE
SCr 1.5-fold increase; GFR 25% decrease
SCr 2-fold increase; GFR 50% decrease
Loss of kidney function (need for RRT) for 4 weeks
Loss of kidney function (need for RRT) for 3 months
AKIN
SCr 1.5-fold or 0.3 mg/dL increase
SCr 2-fold increase
KDIGO
SCr 1.5-fold or 0.3 mg/dL increase 0.5 mL/kg/hr for 6 hours
SCr 2-fold increase
SCr 3-fold increase, or GFR 75% decrease, or SCr 4 mg/dL with 0.5 mg/dL acute rise SCr 3-fold increase, or SCr 4 mg/dL with 0.5 mg/dL acute rise SCr 3-fold increase, or Scr 4 mg/dL, or initiation of RRT 0.3 mL/kg/hr for 24 hours or anuria for 12 hours
Urine criteria (common to all definitions)
0.5 mL/kg/hr for 12 hours
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Abbreviations: AKI, acute kidney disease; AKIN, Acute Kidney Injury Network; ESRD, end-stage renal disease; GFR, glomerular filtration rate; KDIGO, Kidney Disease: Improving Global Outcomes; RIFLE, Risk, Injury, Failure; Loss, End-Stage; RRT, renal replacement therapy; SCr, serum creatinine.
Health and Clinical Excellence (NICE) guidelines from the United Kingdom were identified by the search.11 Additionally, the American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines specifically discussing contrast-induced AKI were found and are included in our review.12 The guidelines are extensive and considerations of all issues they address is beyond the scope of our article; instead, the guidelines were examined by the authors and the most salient points have been summarized by consensus.
Results Definition of AKI
Prior to 2004, there was no consensus definition of AKI, and a literature search at that time would have identified . 30 different definitions in use. The lack of uniformity severely hampered proper epidemiologic and clinical studies on causes and treatment of patients with AKI; therefore, establishment of a standard definition was imperative. The Risk, Injury, Failure, Loss, End-stage (RIFLE) criteria were first published nearly a decade ago, providing a unifying definition and staging of AKI based on patients urine output and creatinine changes over a 1-week period (Table 1).13 The Acute Kidney Injury Network (AKIN) modified the RIFLE classification scheme by applying a smaller increment in patient creatinine concentration increase (0.3 mg/dL) over a 48-hour period, based on studies showing that such an increase correlated with increased mortality and morbidity.14 Recently, the KDIGO guideline combined aspects of the RIFLE criteria and AKIN modification by differentiating the time periods during which alternate thresholds of patient creatinine change must occur.10 Using the KDIGO format, AKI is defined as either an absolute serum creatinine increase of 0.3 mg/dL occurring within a 48-hour period, or a 50% increase in
patient serum creatinine level during a 7-day period. Urinary output criteria for AKI are identical in all 3 guidelines, RIFLE, AKIN, and KDIGO. The ATS guidelines, published before release of the KDIGO criteria, recommended use of either the RIFLE or AKIN criteria.8 Both the draft NICE guideline and the UK Renal Association recommend adoption of the KDIGO definition for AKI.9,11 The utility of the new classifications of AKI in predicting morbidity and mortality in hospitalized patients has been demonstrated in . 500 000 patients worldwide in numerous settings, including critical illness, burns, trauma, cancer, cardiovascular surgery, and radiocontrast.15 Although use of a consensus definition of AKI will lead to better designed clinical trials and hopefully, improved patient outcomes, it is still unclear how the related guidelines and recommendations will impact actual clinical care. A small increment in patient serum creatinine that rapidly reverses with simple volume resuscitation likely is not clinically relevant; nor do the new classification schemes account for the pathophysiology of AKI, including pre-renal states, obstruction, and glomerulonephritis. Furthermore, fluctuations in patient hourly urine output have been inconsistently associated with clinical outcomes and are often inaccurate; therefore, adaption of the KDIGO definition of AKI beyond clinical trial design should be made cautiously. In the clinical arena, defining early AKI by KDIGO criteria should be viewed as an initial signal of renal injury, but management of the patient should still depend on clinical status, comorbid conditions, volume status, renal function trend, and the specific cause of AKI.
Renal Ultrasound
Urinary tract obstruction is a well-known but infrequent cause of AKI in hospitalized patients. Renal ultrasound is
8
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Summary of Clinical Practice Guidelines for AKI
often performed to evaluate for the presence of obstruction, however its routine use in the evaluation of AKI has been questioned.16,17 Guidelines on the use of renal ultrasound are vague. In KDIGO, ultrasound is recommended in the evaluation of AKI only if obstruction is suspected, but the guideline provides no specifics.10 The NICE draft guideline on use of renal ultrasound in the workup of AKI is based on a single, retrospective study, and recommends against routine ultrasound if the cause of AKI has already been determined.11,18 If the cause of AKI remains unknown and the patient is at risk for urinary tract obstruction, renal ultrasound within 24 hours is recommended. “Immediate” ultrasound is recommended only when obstructive pyelonephritis is suspected. The UK Renal Association makes a similar recommendation.9 The ATS mentions that obstruction is “easy to rule out” with renal ultrasonography but provides little additional guidance on when the study should be obtained.8 In our recent study on routine use of ultrasound in the evaluation of 810 hospitalized patients for AKI, 1% had hydronephrosis without pre-existing clinical findings suggestive of obstructive nephropathy19; therefore, routine renal ultrasound for the evaluation of AKI is not recommended but should be used in selected patients.
solutions be avoided with no directives for assessing the adequacy of volume repletion.8 The draft NICE guideline provides no recommendations on resuscitation fluid choice.11 Avoidance of hydroxyethyl starches, use of small boluses of isotonic crystalloid, and monitoring patient response to fluids by measuring urine output and central venous pressures are suggested by the UK Renal Association.9 The KDIGO guideline makes 1 specific recommendation: isotonic crystalloids should be used for volume resuscitation in all situations except in patients with hemorrhagic shock.10 It is increasingly recognized that excessive fluid administration can be harmful to patients; however, no specific recommendations for assessment of intravascular volume status are made. Since publication of the guidelines, several studies comparing crystalloids and colloids have been published. What has become clear is that colloids have not been proven superior to crystalloids in terms of clinically meaningful patient outcomes and are more costly. Given the fact that some harm has been reported with the use of starches, crystalloid solutions for initial volume resuscitation is appropriate. This approach is included in the 2012 Surviving Sepsis Guidelines.23
Volume Resuscitation
Vasodilators
Reduced renal perfusion is frequently a contributing cause of AKI and volume resuscitation is the primary intervention, thus proper use of intravenous (IV) fluids is a fundamental concept in the care of patients with AKI. Determining the appropriate amount and composition of resuscitation fluids remains a challenge. Crystalloids are aqueous solutions of mineral salts, such as 0.9% saline and lactated Ringer’s solution. Colloids are defined as high molecular weight substances that are mainly confined to the intravascular space and include human albumin, dextrans, hydroxyethyl starches, and gelatin plasma substitutes. Although arguments have been made suggesting that colloidal agents are preferable to crystalloid solutions as volume expanders because they are confined to the vascular space, multiple studies have failed to support this contention. In fact, several recent trials have shown increased risk of patient mortality or need for renal replacement therapies (RRTs) in patients who received various hydroxyethyl starches compared with those receiving crystalloid solutions.20–22 The ATS guidelines antedate several of the newer trials and meta-analyses demonstrating the negative effects of hydroxyethyl starch, and recommended that hyper-oncotic
Prevention of AKI Dopamine Low-dose dopamine administration (1–3 µg/kg/min) to healthy individuals causes renal vasodilation, natriuresis, and increased glomerular filtration rate (GFR); because of these effects, dopamine has been given for prevention of AKI in numerous clinical settings. Most positive trials have been small, inadequately randomized, of limited statistical power, and with endpoints of questionable clinical significance.24,25 However, more recent randomized trials of sufficient power have shown that low-dose dopamine is not effective in preventing AKI.26–28 The KGIDO guideline strongly recommends against using low-dose dopamine to prevent or treat patients with AKI.10 The NICE guidelines state there is a lack of evidence for the efficacy of low-dose dopamine therapy, whereas the UK Renal Association guidelines state that it is of no therapeutic benefit to patients and may be associated with harm.9,11 Fenoldopam Fenoldopam is a selective dopamine receptor agonist approved for use as a parenteral anti-hypertensive agent. Both animal studies and small clinical trials have suggested that fenoldopam may be effective in preventing or ameliorating
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early AKI in sepsis and post-cardiac surgery although in a large randomized control study, use of fenoldopam failed to prevent AKI resulting from radiocontrast administration.29–32 Based on available evidence, KDIGO suggests against using fenoldopam to prevent or treat AKI.10 The UK Renal Association guidelines state that the available evidence for fenoldopam use is inconclusive and further studies need to be completed before its use can be recommended.9
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Radiocontrast Administration The high prevalence of intra-arterial and IV radiocontrast administration has led to a high incidence of contrast-induced nephropathy (CIN). Numerous therapeutic strategies have been evaluated to prevent or mitigate CIN, yet controversy still exists regarding proper management. All AKI guidelines recommend an evaluation of risk factors for CIN, such as chronic kidney disease (CKD), diabetes mellitus, or volume depletion prior to administration of radiocontrast. A strong recommendation is made in the KDIGO guidelines for the avoidance of hyperosmolar iodinated contrast and the use of iso- or hypo-osmolar contrast agents instead.10 A similar statement is made in the ATS guideline.8 Volume Expansion Volume expansion with IV fluids is the most frequently used therapy for preventing CIN and the approach is endorsed by KDIGO.10 Either isotonic saline or bicarbonate solutions are recommended by both KDIGO and the UK Renal Association. 9 The draft NICE guideline similarly recommends isotonic saline or bicarbonate be administered to patients receiving radiocontrast who either are at risk of CIN or acutely ill.11 The ATS guideline is more circumspect regarding IV fluids, recommending that volume status be optimized before contrast administration, and that isotonic sodium bicarbonate infusion be considered first. 8 The ACCF/AHA 2011 guideline update on unstable angina/NSTEMI management added a similar qualitative statement recommending “adequate preparatory hydration” in patients with CKD undergoing coronary angiography.12 N-acetylcysteine N-acetylcysteine (NAC), a pro-drug of L-cysteine, replenishes glutathione stores and is approved for use in the treatment of patients with acetaminophen intoxication. Use of NAC has also been extensively investigated in the prevention of CIN because of its vasodilatory and
antioxidant properties. Previous trials supporting the beneficial effects of NAC administration were relatively small and had numerous design flaws.33 More recently, the Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT) tested high-dose oral NAC use in a large number of patients at risk for CIN undergoing coronary or percutaneous angiography, and found no benefit in terms of reducing developing AKI34; nevertheless, given the significance of CIN and prior meta-analyses suggesting a benefit from NAC treatment, as well as its safety and low cost, many practitioners continue to use it in clinical practice.35 This line of reasoning is reflected in the KDIGO guidelines, which make a recommendation for oral NAC as a “suggestion,” based on “very low” quality evidence which “often will be far from the truth.”10 The ATS guidelines are even less supportive about the utility of NAC for prevention of CIN in critically ill patients, suggesting that NAC therapy may be considered but cannot be recommended because of insufficient evidence.8 The ACCF/AHA guideline makes no recommendation regarding NAC, again citing a lack of evidence.12 The draft NICE guidelines recommend oral or IV NAC be considered before radiocontrast is given.11 “No compelling evidence for the routine use of NAC” to prevent CIN is the judgment of the UK Renal Association guideline authors.9 Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are frequently prescribed antihypertensive medications that alter patient renal hemodynamics and may predispose to AKI in some circumstances. Clinicians are often faced with the question of whether to continue ACE inhibitors/ARB therapy in patients who are to receive radiocontrast. The KDIGO authors commented that there is no compelling evidence to recommend holding ACE inhibitors/ARB therapy prior to administration.10 The same conclusion was reached in the draft NICE and UK Renal Association guidelines.9,11 Studies using extracorporeal renal support (hemodialysis or hemofiltration) to prevent CIN were reviewed by the KDIGO authors and they concluded that although there is some low-quality evidence of benefit of extracorporeal therapy to prevent CIN, given the costs and uncertain risk– benefit profile, these procedures are not recommended.10,36–39 Guidelines for the prevention of CIN in patients are outlined in Table 2.
Treatment of Patients With AKI
No effective treatment exists for patients with established AKI. Although numerous animal studies have identified
10
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Summary of Clinical Practice Guidelines for AKI
Table 2. Prevention of CIN KDIGO
ATS
ACCF/AHA
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UK Renal Association NICE
Consider alternative imaging method Use lowest contrast dose Use iso-osmolar or low-osmolar iodinated contrast Volume expansion with isotonic crystalloid (either sodium chloride or sodium bicarbonate) Use oral NAC Do not use prophylactic hemodialysis or hemofiltration Use iso-osmolar or low-osmolar iodinated contrast Consider holding nephrotoxic medications Optimize volume status Consider isotonic sodium bicarbonate administration Consider intravenous NAC Adequate preparatory hydration Contrast volume should be adjusted based on CrCl Pre-procedure volume expansion with isotonic sodium chloride or sodium bicarbonate Volume expansion with isotonic sodium chloride or sodium bicarbonate Consider oral or IV NAC Discuss care with nephrology team
Abbreviations: ACCF, American College of Cardiology Foundation; AHA, American Heart Association; ATS, American Thoracic Society; CIN, contrast-induced neuropathy; CrCL, creatinine clearance; IV, intravenous; KDIGO, Kidney Disease: Improving Global Outcomes; NAC, N-acetylcysteine; NICE, National Institute for Health and Clinical Excellence.
s everal agents that ameliorate renal injury, none have improved human disease. The discordance has been attributed to poor animal models of AKI and delayed therapy in humans. Although the explanation is valid, lack of clinical benefit in human studies also reflects our limited understanding of the pathophysiology of AKI.
Mannitol Mannitol has been used frequently in the past for prevention and treatment of AKI; however, most of the studies are retrospective and underpowered.46,47 Based on review of past study data, the KDIGO group concluded that use of mannitol was not scientifically justified.10 Mannitol use in patients with AKI is not addressed by the other guidelines.
Diuretics Loop Diuretics Loop diuretics (furosemide, bumetanide, torsemide) were long considered beneficial in the treatment of patients with AKI by maintaining urinary flow to prevent intratubular cast formation and reducing oxygen consumption by the thick ascending loop of Henle.40,41 However, clinical trials have shown loop diuretics are not effective in treating patients with AKI and are possibly harmful.42–44 Use of loop diuretics increases the luminal concentration of sodium and may increase production of the tubular Tamm-Horsfall protein and paradoxically, increase cast formation.45 The KDIGO guideline recommends against using loop diuretics to treat patients with AKI and to only use them in established AKI to treat hypervolemia.10 The ATS guideline recommends that following volume resuscitation in AKI, loop diuretics may be given for testing renal responsiveness, even though the guideline notes that loop diuretics have not shown benefit in decreasing patient morbidity or mortality.8 The NICE draft guideline and the UK Renal Association come to similar conclusions as KDIGO: loop diuretics should only be used in patients with AKI for treatment of volume overload.9,11
Natriuretic Peptides Natriuretic peptides are released from the cardiac atria (atrial natriuretic peptide, ANP) and ventricles (brain natriuretic peptide, BNP) in response to cardiac stretch and volume overload. Because natriuretic peptides alter renal vascular tone and promote natriuresis (increased urinary sodium loss), there has been a keen interest in the use of recombinant natriuretic peptides for the management of cardiac and renal dysfunction. The KDIGO guideline is against the use of ANP(anaritide) for the treatment of AKI based on a review of several negative clinical trials.10 The KDIGO guideline also examined available data for BNP (nesiritide) but made no recommendations regarding therapeutic use of the agent. The ATS guideline only mention anaritide by recommending further research into its possible therapeutic use. No comment on use of natriuretic peptides is made by the draft NICE or the UK Renal Association guidelines. Subsequent to the publication of the mentioned guidelines, in a study of 360 patients with acute decompensated heart failure and renal dysfunction, the addition of either continuous infusion of low-dose dopamine or nesiritide to standard diuretic therapy did not improve fluid removal or renal function.48
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Other Agents The use of other hormonal agents for prevention or treatment of AKI is also addressed briefly in the KDIGO guideline,10 which recommends against the use of insulin-like growth factor 1 for AKI based on lack of efficacy in human studies and mentions that studies on the use of erythropoietin for AKI are equivocal and its use is not recommended as well.
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Renal Replacement Therapy
Although all clinicians agree on when RRT must commence (indications for dialysis), controversy still surrounds many issues use of RRT in patients without emergent indications, including the parameters of timing of initiation, mode of RRT (intermittent or continuous), and dose.
Timing Only 1 RCT controlled trial has assessed the effects of early versus traditional initiation of RRT in patients with AKI, and the study, which had negative findings, was significantly underpowered49; all other studies to date have been observational analyses, which suggest a survival advantage for patients with earlier RRT.50–53 The KDIGO guideline starts with a commonsense recommendation that RRT should be initiated emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist.10 The clinical context, laboratory trends, and other considerations should guide decisions on when to start RRT, rather than reliance on single blood urea nitrogen (BUN) or creatinine values. The ATS also makes basic recommendations by listing common indications for RRT, such as to improve metabolic or electrolyte abnormalities, and allowing administration of copious volumes of therapeutic fluids.8 The ATS also states that RRT may be appropriate earlier in the course of AKI, before “traditional” threshold laboratory or clinical parameters are met, because of the fragility of critically ill patients. The NICE draft makes similar statements about the importance of evaluating the entire clinical picture and not simply relying on isolated patient laboratory values.11
Modality Renal replacement therapy can be broadly divided into 2 forms, continuous (CRRT) and intermittent. As CRRT removes fluid and solute more slowly than intermittent therapies during a 24-hour period, it has been considered a superior modality for unstable, critically ill patients; however, most randomized trials have failed to clearly show this superiority.54,55 The multiple guidelines reflect this uncertainty. Recommendations from the KDIGO guideline regarding modality
of renal support point to the absence of a clearly superior modality,10 and suggest that CRRT and intermittent treatments should be used as complementary therapies while pointing out that meta-analyses have failed to show the superiority of CRRT for important outcomes, such as patient mortality or impact on length of hospital or intensive care unit stay. The KDIGO guideline states that CRRT is preferred to intermittent therapy for patients with hemodynamic instability because some studies have shown higher mean arterial pressure and less vasopressor use with CRRT compared with intermittent treatments56; KDIGO also suggests that CRRT is preferred in cases where patients have acute brain injury, cerebral edema, or intracranial hypertension because small studies have shown increased intracranial pressure and increased cerebral water content following intermittent therapy compared with CRRT.56,57 The ATS guideline comes to largely the same conclusions as the KDIGO group, emphasizing the importance of individual patient variables affecting the choice of mode and suggesting CRRT for patients with brain edema, severe hemodynamic instability, ongoing metabolic acidosis, and high-volume removal needs.8
Dialysis Dose The concept of dose of dialysis is firmly established in patients with CKD. Using urea removal as a surrogate of overall clearance of metabolic waste, adequacy of dose is achieved when patient pre-dialysis BUN level is reduced by $ 65% or a unit-less measure of urea clearance, KT/V, is . 1.2. Until recently, what constituted an adequate dose of dialysis in hospitalized and critically ill patients, including those on CRRT, had not been established.58–60 The KDIGO guideline recommends that the dose of RRT should be determined and prescribed appropriately before the treatment is started.10 Another recommendation is to assess dialysis dose delivered and adjust the patient prescription as necessary to achieve desired dose. Based on results of the Veterans Affairs/ National Institutes of Health-sponsored Acute Renal Failure Trial Network (ATN) study, it was recommended that a KT/V of 3.9 per week be delivered in patients with AKI receiving intermittent dialysis (assuming 3-times weekly treatment), and an effluent volume of 20 to 25 mL/kg/hour be delivered by CRRT.61 The ATS guideline made similar recommendations regarding dose: weekly KT/V of 3.6 for intermittent therapies, and delivered effluent volume of . 20 mL/kg/hour for continuous modalities.8 It is important to note that the recommended doses are the minimum required and that they must be delivered and not merely prescribed.
12
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Discussion
Acute kidney injury remains a significant health care issue associated with high patient morbidity and mortality. Extensive practice guidelines have now been published regarding diagnosis, prevention, and treatment of AKI. We have summarized the salient features in Table 3. Current guidelines are a great start to improving clinical research, and eventually patient outcomes, however, they are not without shortcomings. First, many of the recommendations are based on rather weak evidence given the lack of RCTs. Second, because of an incomplete understanding of the pathophysiology of AKI, very few prevention and treatment trials have targeted mechanisms of injury rather than nonspecific parameters, such as renal blood flow and urinary output. Finally, some recommendations, such as the definition of AKI, are mainly relevant to the design of clinical trials. Whether the use of the KDIGO definition of AKI in the clinical setting actually will improve outcomes is unknown. Although beyond the scope of our review, several critiques of the KDIGO guidelines are available.62,63
Conflict of Interest Statement
Carl P. Walther, MD, and Amber S. Podoll, MD, FACP, disclose no conflicts of interest. Kevin W. Finkel, MD, FACP, FASN, FCCM, is a member of the advisory committee/board of NxStage Corporation, and has received research funding from Thrasos Pharma and Spectral Diagnostics. Table 3. Summary Guidelines for AKI • AKI should be defined by KDIGO criteria; however, patient management should still be guided by overall clinical status, comorbid conditions, renal function trend, volume status, and etiology of AKI • Renal ultrasound is not recommended for routine evaluation of AKI but should be utilized when the clinical suspicion of obstruction is high • Crystalloid solutions should be used for volume resuscitation and are preferred over colloid solutions • Low-dose dopamine and fenoldopam are not recommended for the prevention or treatment of AKI • Diuretics (loop diuretics and mannitol) are not recommended for the prevention or treatment of AKI. Loop diuretics are indicated for treatment of volume overload in the face of AKI • Natriuretic peptides are not recommended for the prevention or treatment of AKI • Dialysis should be initiated based on the clinical scenario rather than on specific laboratory features • CRRT and intermittent therapies should be considered complementary modalities. CRRT may be more appropriate in patients with hemodynamic instability, head injury, or cerebral edema • A minimum adequate dose of dialysis should be delivered as a weekly KT/V of 3.9 for intermittent dialysis and 25 mL/kg/hr for CRRT Abbreviations: AKI, acute kidney injury; CRRT, continuous renal replacement; KDIGO, Kidney Disease, Improving Global Outcomes.
References 1. Wang HE, Muntner P, Chertow GM, Warnock DG. Acute kidney injury and mortality in hospitalized patients. Am J Nephrol. 2012; 35(4):349–355. 2. Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DW. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. 2005;16(11):3365–3370. 3. Shihab FS. Preconditioning: from experimental findings to novel therapies in acute kidney injury. Minerva Urol Nefrol. 2009;61(3):143–157. 4. Jo SK, Rosner MH, Okusa MD. Pharmacologic treatment of acute kidney injury: why drugs haven’t worked and what is on the horizon. Clin J Am Soc Nephrol. 2007;2(2):356–365. 5. Han X, Zhao L, Lu G, et al. Improving outcomes of acute kidney injury using mouse renal progenitor cells alone or in combination with erythropoietin or suramin. Stem Cell Res Ther. 2013;4:74. 6. Clark E, Wald R, Walsh M, Bagshaw SM, Canadian Acute Kidney Injury (CANAKI) Investigators. Timing of initiation of renal replacement therapy for acute kidney injury: a survey of nephrologists and intensivists in Canada. Nephrol Dial Transplant. 2012;27(7):2761–2767. 7. Uchino S, Bellomo R, Morimatsu H, et al. Discontinuation of continuous renal replacement therapy: a post hoc analysis of a prospective multicenter observational study. Crit Care Med. 2009;37(9):2576–2582. 8. Brochard L, Abroug F, Brenner M, et al; ATS/ERS/ESICM/SRLF Ad Hoc Committee on Acute Renal Failure. An Official ATS/ERS/ ESICM/SCCM/SRLF Statement: Prevention and Management of Acute Renal Failure in the ICU Patient: an international consensus conference in intensive care medicine. Am J Respir Crit Care Med. 2010;181(10):1128–1155. 9. Lewington A, Kanagasundaram S. Renal Association Clinical Practice Guidelines on acute kidney injury. Nephron Clin Pract. 2011; 118(Suppl 1):c349–c390. 10. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int. 2012;2(1):1–138. 11. Excellence NHaC. Acute kidney injury: Prevention, detection, and management up to the point of renal replacement therapy. London: National Institute for Health and Care Excellence, 2013. 12. 2011 ACCF/AHA Focused Update of the Guidelines for the Management of Patients With Unstable Angina/ Non-ST-Elevation Myocardial Infarction (Updating the 2007 Guideline): a Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2011;123(18):2022–2060. 13. Bellomo R, Ronco C, Kellum JA, Mehta RL, Palevsky P; Acute Dialysis Quality Initiative Workgroup. Acute renal failure — definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8(4):R204–R212. 14. Mehta RL, Kellum JA, Shah SV, et al; Acute Kidney Injury Network. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31. 15. Srisawat N, Hoste EE, Kellum JA. Modern classification of acute kidney injury. Blood Purif. 2010;29(3):300–307. 16. Gottlieb RH, Weinberg EP, Rubens DJ, Monk RD, Grossman EB. Renal sonography: can it be used more selectively in the setting of an elevated serum creatinine level? Am J Kidney Dis. 1997;29(3):362–367. 17. Ritchie WW, Vick CW, Glocheski SK, Cook DE. Evaluation of azotemic patients: diagnostic yield of initial US examination. Radiology. 1988;167(1):245–247. 18. Licurse A, Kim MC, Dziura J, et al. Renal ultrasonography in the evaluation of acute kidney injury: developing a risk stratification framework. Arch Intern Med. 2010;170(21):1900–1907. 19. Podoll A, Walther C, Finkel K. Clinical utility of gray scale renal ultrasound in acute kidney injury. BMC Nephrol. 2013;14:188. 20. Haase N, Perner A, Hennings LI, et al. Hydroxyethyl starch 130/0.38–0.45 versus crystalloid or albumin in patients with sepsis: systematic review with meta-analysis and trial sequential analysis. BMJ. 2013;346:f839.
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Walther et al 21. Zarychanski R, Abou-Setta AM, Turgeon AF, et al. Association of hydroxyethyl starch administration with mortality and acute kidney injury in critically ill patients requiring volume resuscitation: a systematic review and meta-analysis. JAMA. 2013;309(7):678–688. 22. Yunos NM, Bellomo R, Hegarty C, Story D, Ho L, Bailey M. Association between a chloride-liberal vs chloride-restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA. 2012;308(15):1566–1572. 23. Dellinger RP, Levy MM, Rhodes A, et al; Surviving Sepsis Campaign Guidelines Committee including the Pediatric Subgroup. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41(2):580–637. 24. Cuthbertson BH, Noble DW. Dopamine in oliguria. BMJ. 1997; 314(7082):690–691. 25. Kapoor A, Sinha N, Sharma RK, et al. Use of dopamine in the prevention of contrast induced acute renal failure. Int J Cardiol. 1996; 53(3):233–236. 26. Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet. 2000;356(9248):2139–2143. 27. Lauschke A, Teichgraber UK, Frei U, Eckardt KU. ‘Low-dose’ dopamine worsens renal perfusion in patients with acute renal failure. Kidney Int. 2006;69(9):1669–1674. 28. Marik PE. Low-dose dopamine: a systematic review. Intensive Care Med. 2002;28(7):877–883. 29. Murray PT. Fenoldopam: renal-dose dopamine redux? Crit Care Med. 2006;34(3):910–911. 30. Cogliati AA, Vellutini R, Nardini A, et al. Fenoldopam infusion for renal protection in high-risk cardiac surgery patients: a randomized clinical study. J Cardiothorac Vasc Anesth. 2007;21(6):847–850. 31. Tumlin JA, Finkel KW, Murray PT, Samuels J, Cotsonis G, Shaw AD. Fenoldopam mesylate in early acute tubular necrosis: a randomized, double-blind, placebo-controlled clinical trial. Am J Kidney Dis. 2005;46(1):26–34. 32. Stone GW, McCullough PA, Tumlin JA, et al; CONTRAST Investigators. Fenoldopam mesylate for the prevention of contrast-induced nephropathy: a randomized controlled trial. JAMA. 2003;290(17):2284–2291. 33. McCullough PA. Contrast-induced acute kidney injury. J Am Coll Cardiol. 2008;51(15):1419–1428. 34. Kelly AM, Dwamena B, Cronin P, Bernstein SJ, Carlos RC. Meta-analysis: effectiveness of drugs for preventing contrast-induced nephropathy. Ann Intern Med. 2008;148(4):284–294. 35. ACT Investigators. Acetylcysteine for prevention of renal outcomes in patients undergoing coronary and peripheral vascular angiography: main results from the randomized Acetylcysteine for Contrast-induced nephropathy Trial (ACT). Circulation. 2011;124(11):1250–1259. 36. Marenzi G, Lauri G, Campodonico J, et al. Comparison of two hemofiltration protocols for prevention of contrast-induced nephropathy in high-risk patients. Am J Med. 2006;119(2):155–162. 37. Marenzi G, Marana I, Lauri G, et al. The prevention of radiocontrast-agent-induced nephropathy by hemofiltration. N Engl J Med. 2003;349(14):1333–1340. 38. Deray G. Dialysis and iodinated contrast media. Kidney Int. 2006;100(Suppl):S25–S29. 39. Vogt B, Ferrari P, Schonholzer C, et al. Prophylactic hemodialysis after radiocontrast media in patients with renal insufficiency is potentially harmful. Am J Med. 2001;111(9):692–698. 40. Ludens JH, Hook JB, Brody MJ, Williamson HE. Enhancement of renal blood flow by furosemide. J Pharmacol Exp Ther. 1968;163(2): 456–460. 41. Ludens JH, Williamson HE. Effect of furosemide on renal blood flow in the conscious dog. Proc Soc Exp Biol Med. 1970;133(2):513–515. 42. Mehta RL, Pascual MT, Soroko S, Chertow GM; PICARD Study Group. Diuretics, mortality, and nonrecovery of renal function in acute renal failure. JAMA. 2002;288(20):2547–2553.
43. Lassnigg A, Donner E, Grubhofer G, Presterl E, Druml W, Hiesmayr M. Lack of renoprotective effects of dopamine and furosemide during cardiac surgery. J Am Soc Nephrol. 2000;11(1):97–104. 44. Lombardi R, Ferreiro A, Servetto C. Renal function after cardiac surgery: adverse effect of furosemide. Ren Fail. 2003;25(5):775–786. 45. Ying WZ, Sanders PW. Dietary salt modulates renal production of transforming growth factor-beta in rats. Am J Physiol. 1998;274(4 Pt 2): F635–F641. 46. Shilliday I, Allison ME. Diuretics in acute renal failure. Ren Fail. 1994; 16(1):3–17. 47. Majdumdar SR, Kjellstrand CM. Why do we use diuretics in acute renal failure? Semin Dial. 1996;9(6):454–459. 48. Chen HH, Anstrom KJ, Givertz MM, et al; for the NHLBI Heart Failure Clinical Research Network. Low-Dose Dopamine or Low-Dose Nesiritide in Acute Heart Failure With Renal Dysfunction: The ROSE Acute Heart Failure Randomized Trial [published online ahead of print November 18, 2013]. JAMA. doi:10.1001/jama.2013.282190. 49. Bouman CS, Oudemans-Van Straaten HM, Tijssen JG, Zandstra DF, Kesecioglu J. Effects of early high-volume continuous venovenous hemofiltration on survival and recovery of renal function in intensive care patients with acute renal failure: a prospective, randomized trial. Crit Care Med. 2002;30(10):2205–2211. 50. Liu KD, Himmelfarb J, Paganini E, et al. Timing of initiation of dialysis in critically ill patients with acute kidney injury. Clin J Am Soc Nephrol. 2006;1(5):915–919. 51. Elahi MM, Lim MY, Joseph RN, Dhannapuneni RR, Spyt TJ. Early hemofiltration improves survival in post-cardiotomy patients with acute renal failure. Eur J Cardiothorac Surg. 2004;26(5):1027–1031. 52. Demirkilic U, Kuralay E, Yenicesu M, et al. Timing of replacement therapy for acute renal failure after cardiac surgery. J Card Surg. 2004;19(1):17–20. 53. Bagshaw SM, Uchino S, Bellomo R, et al; Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Timing of renal replacement therapy and clinical outcomes in critically ill patients with severe acute kidney injury. J Crit Care. 2009;24(1):129–140. 54. Rabindranath K, Adams J, Macleod AM, Muirhead N. Intermittent versus continuous renal replacement therapy for acute renal failure in adults. Cochrane Database Syst Rev. 2007;(3):CD003773. 55 Bagshaw SM, Berthiaume LR, Delaney A, Bellomo R. Continuous versus intermittent renal replacement therapy for critically ill patients with acute kidney injury: a meta-analysis. Crit Care Med. 2008;36(2):610–617. 56. Bagshaw SM, Peets AD, Hameed M, Boiteau PJ, Laupland KB, Doig CJ. Dialysis Disequilibrium Syndrome: brain death following hemodialysis for metabolic acidosis and acute renal failure—a case report. BMC Nephrol. 2004;5:9. 57. Lin CM, Lin JW, Tsai JT, et al. Intracranial pressure fluctuation during hemodialysis in renal failure patients with intracranial hemorrhage. Acta Neurochir Suppl. 2008;101:141–144. 58. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26–30. 59. Tolwani AJ, Campbell RC, Stofan BS, Lai KR, Oster RA, Wille KM. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233–1238. 60. Schiffl H, Lang SM, Fischer R. Daily hemodialysis and the outcome of acute renal failure. N Engl J Med. 2002;346(5):305–310. 61. VA/NIH Acute Renal Failure Trial Network, Palevsky PM, Zhang JH, O’Connor TZ, et al. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7–20. 62. Palevsky PM, Liu KD, Brophy PD, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. Am J Kidney Dis. 2013;61(5):649–672. 63. James M, Bouchard J, Ho J, et al. Canadian society of nephrology commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. Am J Kidney Dis. 2013;61(5):673–685.
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Summary of Clinical Practice Guidelines for Acute Kidney Injury
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DOI: 10.3810/hp.2014.02.1086
Carl P. Walther, MD 1 Amber S. Podoll, MD, FACP 1 Kevin W. Finkel, MD, FACP, FASN, FCCM 1 1 University of Texas Health Science Center at Houston, Department of Medicine, Division of Renal Diseases and Hypertension, Houston, TX
Abstract: Clinical practice guidelines are intended to standardize the diagnosis and treatment of diseases in order to improve both patient outcomes and resource utilization, using evidence-based criteria. As recently as a decade ago, there was no agreed upon definition of acute kidney injury (AKI), making it difficult to conduct proper clinical studies on the epidemiology and treatment of the disorder. Following the advent of the Risk, Injury, Failure, Loss, and End-stage (RIFLE) criteria for defining AKI, several guidelines for the diagnosis and management of AKI have been developed. In our review, we present a narrative description and comparison of the major published guidelines. Overall, there has been significant agreement among the various guidelines, and each seems well-reasoned and clinically useful. Perhaps the most striking conclusion upon review of the various guidelines is the limited scope of knowledge about optimal management of patients with AKI. Keywords: acute kidney injury; practice guidelines; evidence-based medicine; clinical trials
Introduction
Correspondence: Kevin W. Finkel, MD, FACP, FASN, FCCM, Professor and Director, Division of Renal Diseases and Hypertension, UT Health Science Center at Houston, 6431 Fannin, Houston, TX 77030. Tel: 713-500-6868 Fax: 713-500-6882 E-mail: [email protected]
Acute kidney injury (AKI) is common among hospitalized patients, and is associated with significant morbidity and mortality.1,2 Despite increasing recognition of its associated medical consequences, there remains significant uncertainty regarding optimal management of patients with AKI. Initially, lack of a consistent definition of AKI limited efforts to conduct proper clinical trials and improve patient outcomes. H owever, in recent years, consensus definitions have been developed and widely adopted (Table 1). Most management strategies for AKI are best described as “supportive care,” and rarely is established AKI remediable through specific interventions.3–5 Renal replacement therapy (often referred to as “renal support” in recognition of the inability to fully replace kidney function), is an active area of research because issues such as timing, modality, and dose remain controversial.6,7 Similarly, several questions remain regarding prevention and management of AKI, including adequacy of volume resuscitation, type of resuscitation fluid (colloid versus crystalloid), and use of various pharmacologic agents (n-acetyl-cysteine, sodium bicarbonate, dopamine agonists, and natriuretic peptides). Therefore, there is a great need for clinical practice guidelines in the field of AKI.
Materials and Methods
Published guidelines on the diagnosis and management of AKI were located through an electronic search of PubMed, Cochrane Reviews, and medical society web pages. The 2010 American Thoracic Society (ATS) guideline,8 the 2011 Renal Association United Kingdom (UK) guideline,9 the 2012 Kidney Disease Improving Global Outcomes (KDIGO) guideline,10 and a draft released in 2013 of proposed National Institute for
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Table 1. AKI Staging Context
RIFLE-Risk AKIN/KDIGO-1
RIFLE-Injury AKIN/KDIGO-3
RIFLE-Failure AKIN/KDIGO-3
RIFLE-Loss
RIFLE-ESRD
RIFLE
SCr 1.5-fold increase; GFR 25% decrease
SCr 2-fold increase; GFR 50% decrease
Loss of kidney function (need for RRT) for 4 weeks
Loss of kidney function (need for RRT) for 3 months
AKIN
SCr 1.5-fold or 0.3 mg/dL increase
SCr 2-fold increase
KDIGO
SCr 1.5-fold or 0.3 mg/dL increase 0.5 mL/kg/hr for 6 hours
SCr 2-fold increase
SCr 3-fold increase, or GFR 75% decrease, or SCr 4 mg/dL with 0.5 mg/dL acute rise SCr 3-fold increase, or SCr 4 mg/dL with 0.5 mg/dL acute rise SCr 3-fold increase, or Scr 4 mg/dL, or initiation of RRT 0.3 mL/kg/hr for 24 hours or anuria for 12 hours
Urine criteria (common to all definitions)
0.5 mL/kg/hr for 12 hours
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Abbreviations: AKI, acute kidney disease; AKIN, Acute Kidney Injury Network; ESRD, end-stage renal disease; GFR, glomerular filtration rate; KDIGO, Kidney Disease: Improving Global Outcomes; RIFLE, Risk, Injury, Failure; Loss, End-Stage; RRT, renal replacement therapy; SCr, serum creatinine.
Health and Clinical Excellence (NICE) guidelines from the United Kingdom were identified by the search.11 Additionally, the American College of Cardiology Foundation/American Heart Association (ACCF/AHA) guidelines specifically discussing contrast-induced AKI were found and are included in our review.12 The guidelines are extensive and considerations of all issues they address is beyond the scope of our article; instead, the guidelines were examined by the authors and the most salient points have been summarized by consensus.
Results Definition of AKI
Prior to 2004, there was no consensus definition of AKI, and a literature search at that time would have identified . 30 different definitions in use. The lack of uniformity severely hampered proper epidemiologic and clinical studies on causes and treatment of patients with AKI; therefore, establishment of a standard definition was imperative. The Risk, Injury, Failure, Loss, End-stage (RIFLE) criteria were first published nearly a decade ago, providing a unifying definition and staging of AKI based on patients urine output and creatinine changes over a 1-week period (Table 1).13 The Acute Kidney Injury Network (AKIN) modified the RIFLE classification scheme by applying a smaller increment in patient creatinine concentration increase (0.3 mg/dL) over a 48-hour period, based on studies showing that such an increase correlated with increased mortality and morbidity.14 Recently, the KDIGO guideline combined aspects of the RIFLE criteria and AKIN modification by differentiating the time periods during which alternate thresholds of patient creatinine change must occur.10 Using the KDIGO format, AKI is defined as either an absolute serum creatinine increase of 0.3 mg/dL occurring within a 48-hour period, or a 50% increase in
patient serum creatinine level during a 7-day period. Urinary output criteria for AKI are identical in all 3 guidelines, RIFLE, AKIN, and KDIGO. The ATS guidelines, published before release of the KDIGO criteria, recommended use of either the RIFLE or AKIN criteria.8 Both the draft NICE guideline and the UK Renal Association recommend adoption of the KDIGO definition for AKI.9,11 The utility of the new classifications of AKI in predicting morbidity and mortality in hospitalized patients has been demonstrated in . 500 000 patients worldwide in numerous settings, including critical illness, burns, trauma, cancer, cardiovascular surgery, and radiocontrast.15 Although use of a consensus definition of AKI will lead to better designed clinical trials and hopefully, improved patient outcomes, it is still unclear how the related guidelines and recommendations will impact actual clinical care. A small increment in patient serum creatinine that rapidly reverses with simple volume resuscitation likely is not clinically relevant; nor do the new classification schemes account for the pathophysiology of AKI, including pre-renal states, obstruction, and glomerulonephritis. Furthermore, fluctuations in patient hourly urine output have been inconsistently associated with clinical outcomes and are often inaccurate; therefore, adaption of the KDIGO definition of AKI beyond clinical trial design should be made cautiously. In the clinical arena, defining early AKI by KDIGO criteria should be viewed as an initial signal of renal injury, but management of the patient should still depend on clinical status, comorbid conditions, volume status, renal function trend, and the specific cause of AKI.
Renal Ultrasound
Urinary tract obstruction is a well-known but infrequent cause of AKI in hospitalized patients. Renal ultrasound is
8
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Summary of Clinical Practice Guidelines for AKI
often performed to evaluate for the presence of obstruction, however its routine use in the evaluation of AKI has been questioned.16,17 Guidelines on the use of renal ultrasound are vague. In KDIGO, ultrasound is recommended in the evaluation of AKI only if obstruction is suspected, but the guideline provides no specifics.10 The NICE draft guideline on use of renal ultrasound in the workup of AKI is based on a single, retrospective study, and recommends against routine ultrasound if the cause of AKI has already been determined.11,18 If the cause of AKI remains unknown and the patient is at risk for urinary tract obstruction, renal ultrasound within 24 hours is recommended. “Immediate” ultrasound is recommended only when obstructive pyelonephritis is suspected. The UK Renal Association makes a similar recommendation.9 The ATS mentions that obstruction is “easy to rule out” with renal ultrasonography but provides little additional guidance on when the study should be obtained.8 In our recent study on routine use of ultrasound in the evaluation of 810 hospitalized patients for AKI, 1% had hydronephrosis without pre-existing clinical findings suggestive of obstructive nephropathy19; therefore, routine renal ultrasound for the evaluation of AKI is not recommended but should be used in selected patients.
solutions be avoided with no directives for assessing the adequacy of volume repletion.8 The draft NICE guideline provides no recommendations on resuscitation fluid choice.11 Avoidance of hydroxyethyl starches, use of small boluses of isotonic crystalloid, and monitoring patient response to fluids by measuring urine output and central venous pressures are suggested by the UK Renal Association.9 The KDIGO guideline makes 1 specific recommendation: isotonic crystalloids should be used for volume resuscitation in all situations except in patients with hemorrhagic shock.10 It is increasingly recognized that excessive fluid administration can be harmful to patients; however, no specific recommendations for assessment of intravascular volume status are made. Since publication of the guidelines, several studies comparing crystalloids and colloids have been published. What has become clear is that colloids have not been proven superior to crystalloids in terms of clinically meaningful patient outcomes and are more costly. Given the fact that some harm has been reported with the use of starches, crystalloid solutions for initial volume resuscitation is appropriate. This approach is included in the 2012 Surviving Sepsis Guidelines.23
Volume Resuscitation
Vasodilators
Reduced renal perfusion is frequently a contributing cause of AKI and volume resuscitation is the primary intervention, thus proper use of intravenous (IV) fluids is a fundamental concept in the care of patients with AKI. Determining the appropriate amount and composition of resuscitation fluids remains a challenge. Crystalloids are aqueous solutions of mineral salts, such as 0.9% saline and lactated Ringer’s solution. Colloids are defined as high molecular weight substances that are mainly confined to the intravascular space and include human albumin, dextrans, hydroxyethyl starches, and gelatin plasma substitutes. Although arguments have been made suggesting that colloidal agents are preferable to crystalloid solutions as volume expanders because they are confined to the vascular space, multiple studies have failed to support this contention. In fact, several recent trials have shown increased risk of patient mortality or need for renal replacement therapies (RRTs) in patients who received various hydroxyethyl starches compared with those receiving crystalloid solutions.20–22 The ATS guidelines antedate several of the newer trials and meta-analyses demonstrating the negative effects of hydroxyethyl starch, and recommended that hyper-oncotic
Prevention of AKI Dopamine Low-dose dopamine administration (1–3 µg/kg/min) to healthy individuals causes renal vasodilation, natriuresis, and increased glomerular filtration rate (GFR); because of these effects, dopamine has been given for prevention of AKI in numerous clinical settings. Most positive trials have been small, inadequately randomized, of limited statistical power, and with endpoints of questionable clinical significance.24,25 However, more recent randomized trials of sufficient power have shown that low-dose dopamine is not effective in preventing AKI.26–28 The KGIDO guideline strongly recommends against using low-dose dopamine to prevent or treat patients with AKI.10 The NICE guidelines state there is a lack of evidence for the efficacy of low-dose dopamine therapy, whereas the UK Renal Association guidelines state that it is of no therapeutic benefit to patients and may be associated with harm.9,11 Fenoldopam Fenoldopam is a selective dopamine receptor agonist approved for use as a parenteral anti-hypertensive agent. Both animal studies and small clinical trials have suggested that fenoldopam may be effective in preventing or ameliorating
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early AKI in sepsis and post-cardiac surgery although in a large randomized control study, use of fenoldopam failed to prevent AKI resulting from radiocontrast administration.29–32 Based on available evidence, KDIGO suggests against using fenoldopam to prevent or treat AKI.10 The UK Renal Association guidelines state that the available evidence for fenoldopam use is inconclusive and further studies need to be completed before its use can be recommended.9
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Radiocontrast Administration The high prevalence of intra-arterial and IV radiocontrast administration has led to a high incidence of contrast-induced nephropathy (CIN). Numerous therapeutic strategies have been evaluated to prevent or mitigate CIN, yet controversy still exists regarding proper management. All AKI guidelines recommend an evaluation of risk factors for CIN, such as chronic kidney disease (CKD), diabetes mellitus, or volume depletion prior to administration of radiocontrast. A strong recommendation is made in the KDIGO guidelines for the avoidance of hyperosmolar iodinated contrast and the use of iso- or hypo-osmolar contrast agents instead.10 A similar statement is made in the ATS guideline.8 Volume Expansion Volume expansion with IV fluids is the most frequently used therapy for preventing CIN and the approach is endorsed by KDIGO.10 Either isotonic saline or bicarbonate solutions are recommended by both KDIGO and the UK Renal Association. 9 The draft NICE guideline similarly recommends isotonic saline or bicarbonate be administered to patients receiving radiocontrast who either are at risk of CIN or acutely ill.11 The ATS guideline is more circumspect regarding IV fluids, recommending that volume status be optimized before contrast administration, and that isotonic sodium bicarbonate infusion be considered first. 8 The ACCF/AHA 2011 guideline update on unstable angina/NSTEMI management added a similar qualitative statement recommending “adequate preparatory hydration” in patients with CKD undergoing coronary angiography.12 N-acetylcysteine N-acetylcysteine (NAC), a pro-drug of L-cysteine, replenishes glutathione stores and is approved for use in the treatment of patients with acetaminophen intoxication. Use of NAC has also been extensively investigated in the prevention of CIN because of its vasodilatory and
antioxidant properties. Previous trials supporting the beneficial effects of NAC administration were relatively small and had numerous design flaws.33 More recently, the Acetylcysteine for Contrast-Induced Nephropathy Trial (ACT) tested high-dose oral NAC use in a large number of patients at risk for CIN undergoing coronary or percutaneous angiography, and found no benefit in terms of reducing developing AKI34; nevertheless, given the significance of CIN and prior meta-analyses suggesting a benefit from NAC treatment, as well as its safety and low cost, many practitioners continue to use it in clinical practice.35 This line of reasoning is reflected in the KDIGO guidelines, which make a recommendation for oral NAC as a “suggestion,” based on “very low” quality evidence which “often will be far from the truth.”10 The ATS guidelines are even less supportive about the utility of NAC for prevention of CIN in critically ill patients, suggesting that NAC therapy may be considered but cannot be recommended because of insufficient evidence.8 The ACCF/AHA guideline makes no recommendation regarding NAC, again citing a lack of evidence.12 The draft NICE guidelines recommend oral or IV NAC be considered before radiocontrast is given.11 “No compelling evidence for the routine use of NAC” to prevent CIN is the judgment of the UK Renal Association guideline authors.9 Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are frequently prescribed antihypertensive medications that alter patient renal hemodynamics and may predispose to AKI in some circumstances. Clinicians are often faced with the question of whether to continue ACE inhibitors/ARB therapy in patients who are to receive radiocontrast. The KDIGO authors commented that there is no compelling evidence to recommend holding ACE inhibitors/ARB therapy prior to administration.10 The same conclusion was reached in the draft NICE and UK Renal Association guidelines.9,11 Studies using extracorporeal renal support (hemodialysis or hemofiltration) to prevent CIN were reviewed by the KDIGO authors and they concluded that although there is some low-quality evidence of benefit of extracorporeal therapy to prevent CIN, given the costs and uncertain risk– benefit profile, these procedures are not recommended.10,36–39 Guidelines for the prevention of CIN in patients are outlined in Table 2.
Treatment of Patients With AKI
No effective treatment exists for patients with established AKI. Although numerous animal studies have identified
10
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Table 2. Prevention of CIN KDIGO
ATS
ACCF/AHA
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UK Renal Association NICE
Consider alternative imaging method Use lowest contrast dose Use iso-osmolar or low-osmolar iodinated contrast Volume expansion with isotonic crystalloid (either sodium chloride or sodium bicarbonate) Use oral NAC Do not use prophylactic hemodialysis or hemofiltration Use iso-osmolar or low-osmolar iodinated contrast Consider holding nephrotoxic medications Optimize volume status Consider isotonic sodium bicarbonate administration Consider intravenous NAC Adequate preparatory hydration Contrast volume should be adjusted based on CrCl Pre-procedure volume expansion with isotonic sodium chloride or sodium bicarbonate Volume expansion with isotonic sodium chloride or sodium bicarbonate Consider oral or IV NAC Discuss care with nephrology team
Abbreviations: ACCF, American College of Cardiology Foundation; AHA, American Heart Association; ATS, American Thoracic Society; CIN, contrast-induced neuropathy; CrCL, creatinine clearance; IV, intravenous; KDIGO, Kidney Disease: Improving Global Outcomes; NAC, N-acetylcysteine; NICE, National Institute for Health and Clinical Excellence.
s everal agents that ameliorate renal injury, none have improved human disease. The discordance has been attributed to poor animal models of AKI and delayed therapy in humans. Although the explanation is valid, lack of clinical benefit in human studies also reflects our limited understanding of the pathophysiology of AKI.
Mannitol Mannitol has been used frequently in the past for prevention and treatment of AKI; however, most of the studies are retrospective and underpowered.46,47 Based on review of past study data, the KDIGO group concluded that use of mannitol was not scientifically justified.10 Mannitol use in patients with AKI is not addressed by the other guidelines.
Diuretics Loop Diuretics Loop diuretics (furosemide, bumetanide, torsemide) were long considered beneficial in the treatment of patients with AKI by maintaining urinary flow to prevent intratubular cast formation and reducing oxygen consumption by the thick ascending loop of Henle.40,41 However, clinical trials have shown loop diuretics are not effective in treating patients with AKI and are possibly harmful.42–44 Use of loop diuretics increases the luminal concentration of sodium and may increase production of the tubular Tamm-Horsfall protein and paradoxically, increase cast formation.45 The KDIGO guideline recommends against using loop diuretics to treat patients with AKI and to only use them in established AKI to treat hypervolemia.10 The ATS guideline recommends that following volume resuscitation in AKI, loop diuretics may be given for testing renal responsiveness, even though the guideline notes that loop diuretics have not shown benefit in decreasing patient morbidity or mortality.8 The NICE draft guideline and the UK Renal Association come to similar conclusions as KDIGO: loop diuretics should only be used in patients with AKI for treatment of volume overload.9,11
Natriuretic Peptides Natriuretic peptides are released from the cardiac atria (atrial natriuretic peptide, ANP) and ventricles (brain natriuretic peptide, BNP) in response to cardiac stretch and volume overload. Because natriuretic peptides alter renal vascular tone and promote natriuresis (increased urinary sodium loss), there has been a keen interest in the use of recombinant natriuretic peptides for the management of cardiac and renal dysfunction. The KDIGO guideline is against the use of ANP(anaritide) for the treatment of AKI based on a review of several negative clinical trials.10 The KDIGO guideline also examined available data for BNP (nesiritide) but made no recommendations regarding therapeutic use of the agent. The ATS guideline only mention anaritide by recommending further research into its possible therapeutic use. No comment on use of natriuretic peptides is made by the draft NICE or the UK Renal Association guidelines. Subsequent to the publication of the mentioned guidelines, in a study of 360 patients with acute decompensated heart failure and renal dysfunction, the addition of either continuous infusion of low-dose dopamine or nesiritide to standard diuretic therapy did not improve fluid removal or renal function.48
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Other Agents The use of other hormonal agents for prevention or treatment of AKI is also addressed briefly in the KDIGO guideline,10 which recommends against the use of insulin-like growth factor 1 for AKI based on lack of efficacy in human studies and mentions that studies on the use of erythropoietin for AKI are equivocal and its use is not recommended as well.
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Renal Replacement Therapy
Although all clinicians agree on when RRT must commence (indications for dialysis), controversy still surrounds many issues use of RRT in patients without emergent indications, including the parameters of timing of initiation, mode of RRT (intermittent or continuous), and dose.
Timing Only 1 RCT controlled trial has assessed the effects of early versus traditional initiation of RRT in patients with AKI, and the study, which had negative findings, was significantly underpowered49; all other studies to date have been observational analyses, which suggest a survival advantage for patients with earlier RRT.50–53 The KDIGO guideline starts with a commonsense recommendation that RRT should be initiated emergently when life-threatening changes in fluid, electrolyte, and acid-base balance exist.10 The clinical context, laboratory trends, and other considerations should guide decisions on when to start RRT, rather than reliance on single blood urea nitrogen (BUN) or creatinine values. The ATS also makes basic recommendations by listing common indications for RRT, such as to improve metabolic or electrolyte abnormalities, and allowing administration of copious volumes of therapeutic fluids.8 The ATS also states that RRT may be appropriate earlier in the course of AKI, before “traditional” threshold laboratory or clinical parameters are met, because of the fragility of critically ill patients. The NICE draft makes similar statements about the importance of evaluating the entire clinical picture and not simply relying on isolated patient laboratory values.11
Modality Renal replacement therapy can be broadly divided into 2 forms, continuous (CRRT) and intermittent. As CRRT removes fluid and solute more slowly than intermittent therapies during a 24-hour period, it has been considered a superior modality for unstable, critically ill patients; however, most randomized trials have failed to clearly show this superiority.54,55 The multiple guidelines reflect this uncertainty. Recommendations from the KDIGO guideline regarding modality
of renal support point to the absence of a clearly superior modality,10 and suggest that CRRT and intermittent treatments should be used as complementary therapies while pointing out that meta-analyses have failed to show the superiority of CRRT for important outcomes, such as patient mortality or impact on length of hospital or intensive care unit stay. The KDIGO guideline states that CRRT is preferred to intermittent therapy for patients with hemodynamic instability because some studies have shown higher mean arterial pressure and less vasopressor use with CRRT compared with intermittent treatments56; KDIGO also suggests that CRRT is preferred in cases where patients have acute brain injury, cerebral edema, or intracranial hypertension because small studies have shown increased intracranial pressure and increased cerebral water content following intermittent therapy compared with CRRT.56,57 The ATS guideline comes to largely the same conclusions as the KDIGO group, emphasizing the importance of individual patient variables affecting the choice of mode and suggesting CRRT for patients with brain edema, severe hemodynamic instability, ongoing metabolic acidosis, and high-volume removal needs.8
Dialysis Dose The concept of dose of dialysis is firmly established in patients with CKD. Using urea removal as a surrogate of overall clearance of metabolic waste, adequacy of dose is achieved when patient pre-dialysis BUN level is reduced by $ 65% or a unit-less measure of urea clearance, KT/V, is . 1.2. Until recently, what constituted an adequate dose of dialysis in hospitalized and critically ill patients, including those on CRRT, had not been established.58–60 The KDIGO guideline recommends that the dose of RRT should be determined and prescribed appropriately before the treatment is started.10 Another recommendation is to assess dialysis dose delivered and adjust the patient prescription as necessary to achieve desired dose. Based on results of the Veterans Affairs/ National Institutes of Health-sponsored Acute Renal Failure Trial Network (ATN) study, it was recommended that a KT/V of 3.9 per week be delivered in patients with AKI receiving intermittent dialysis (assuming 3-times weekly treatment), and an effluent volume of 20 to 25 mL/kg/hour be delivered by CRRT.61 The ATS guideline made similar recommendations regarding dose: weekly KT/V of 3.6 for intermittent therapies, and delivered effluent volume of . 20 mL/kg/hour for continuous modalities.8 It is important to note that the recommended doses are the minimum required and that they must be delivered and not merely prescribed.
12
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Discussion
Acute kidney injury remains a significant health care issue associated with high patient morbidity and mortality. Extensive practice guidelines have now been published regarding diagnosis, prevention, and treatment of AKI. We have summarized the salient features in Table 3. Current guidelines are a great start to improving clinical research, and eventually patient outcomes, however, they are not without shortcomings. First, many of the recommendations are based on rather weak evidence given the lack of RCTs. Second, because of an incomplete understanding of the pathophysiology of AKI, very few prevention and treatment trials have targeted mechanisms of injury rather than nonspecific parameters, such as renal blood flow and urinary output. Finally, some recommendations, such as the definition of AKI, are mainly relevant to the design of clinical trials. Whether the use of the KDIGO definition of AKI in the clinical setting actually will improve outcomes is unknown. Although beyond the scope of our review, several critiques of the KDIGO guidelines are available.62,63
Conflict of Interest Statement
Carl P. Walther, MD, and Amber S. Podoll, MD, FACP, disclose no conflicts of interest. Kevin W. Finkel, MD, FACP, FASN, FCCM, is a member of the advisory committee/board of NxStage Corporation, and has received research funding from Thrasos Pharma and Spectral Diagnostics. Table 3. Summary Guidelines for AKI • AKI should be defined by KDIGO criteria; however, patient management should still be guided by overall clinical status, comorbid conditions, renal function trend, volume status, and etiology of AKI • Renal ultrasound is not recommended for routine evaluation of AKI but should be utilized when the clinical suspicion of obstruction is high • Crystalloid solutions should be used for volume resuscitation and are preferred over colloid solutions • Low-dose dopamine and fenoldopam are not recommended for the prevention or treatment of AKI • Diuretics (loop diuretics and mannitol) are not recommended for the prevention or treatment of AKI. Loop diuretics are indicated for treatment of volume overload in the face of AKI • Natriuretic peptides are not recommended for the prevention or treatment of AKI • Dialysis should be initiated based on the clinical scenario rather than on specific laboratory features • CRRT and intermittent therapies should be considered complementary modalities. CRRT may be more appropriate in patients with hemodynamic instability, head injury, or cerebral edema • A minimum adequate dose of dialysis should be delivered as a weekly KT/V of 3.9 for intermittent dialysis and 25 mL/kg/hr for CRRT Abbreviations: AKI, acute kidney injury; CRRT, continuous renal replacement; KDIGO, Kidney Disease, Improving Global Outcomes.
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43. Lassnigg A, Donner E, Grubhofer G, Presterl E, Druml W, Hiesmayr M. Lack of renoprotective effects of dopamine and furosemide during cardiac surgery. J Am Soc Nephrol. 2000;11(1):97–104. 44. Lombardi R, Ferreiro A, Servetto C. Renal function after cardiac surgery: adverse effect of furosemide. Ren Fail. 2003;25(5):775–786. 45. Ying WZ, Sanders PW. Dietary salt modulates renal production of transforming growth factor-beta in rats. Am J Physiol. 1998;274(4 Pt 2): F635–F641. 46. Shilliday I, Allison ME. Diuretics in acute renal failure. Ren Fail. 1994; 16(1):3–17. 47. Majdumdar SR, Kjellstrand CM. Why do we use diuretics in acute renal failure? Semin Dial. 1996;9(6):454–459. 48. Chen HH, Anstrom KJ, Givertz MM, et al; for the NHLBI Heart Failure Clinical Research Network. Low-Dose Dopamine or Low-Dose Nesiritide in Acute Heart Failure With Renal Dysfunction: The ROSE Acute Heart Failure Randomized Trial [published online ahead of print November 18, 2013]. JAMA. doi:10.1001/jama.2013.282190. 49. Bouman CS, Oudemans-Van Straaten HM, Tijssen JG, Zandstra DF, Kesecioglu J. Effects of early high-volume continuous venovenous hemofiltration on survival and recovery of renal function in intensive care patients with acute renal failure: a prospective, randomized trial. Crit Care Med. 2002;30(10):2205–2211. 50. Liu KD, Himmelfarb J, Paganini E, et al. Timing of initiation of dialysis in critically ill patients with acute kidney injury. Clin J Am Soc Nephrol. 2006;1(5):915–919. 51. Elahi MM, Lim MY, Joseph RN, Dhannapuneni RR, Spyt TJ. Early hemofiltration improves survival in post-cardiotomy patients with acute renal failure. Eur J Cardiothorac Surg. 2004;26(5):1027–1031. 52. Demirkilic U, Kuralay E, Yenicesu M, et al. Timing of replacement therapy for acute renal failure after cardiac surgery. J Card Surg. 2004;19(1):17–20. 53. Bagshaw SM, Uchino S, Bellomo R, et al; Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Timing of renal replacement therapy and clinical outcomes in critically ill patients with severe acute kidney injury. J Crit Care. 2009;24(1):129–140. 54. Rabindranath K, Adams J, Macleod AM, Muirhead N. Intermittent versus continuous renal replacement therapy for acute renal failure in adults. Cochrane Database Syst Rev. 2007;(3):CD003773. 55 Bagshaw SM, Berthiaume LR, Delaney A, Bellomo R. Continuous versus intermittent renal replacement therapy for critically ill patients with acute kidney injury: a meta-analysis. Crit Care Med. 2008;36(2):610–617. 56. Bagshaw SM, Peets AD, Hameed M, Boiteau PJ, Laupland KB, Doig CJ. Dialysis Disequilibrium Syndrome: brain death following hemodialysis for metabolic acidosis and acute renal failure—a case report. BMC Nephrol. 2004;5:9. 57. Lin CM, Lin JW, Tsai JT, et al. Intracranial pressure fluctuation during hemodialysis in renal failure patients with intracranial hemorrhage. Acta Neurochir Suppl. 2008;101:141–144. 58. Ronco C, Bellomo R, Homel P, et al. Effects of different doses in continuous veno-venous haemofiltration on outcomes of acute renal failure: a prospective randomised trial. Lancet. 2000;356(9223):26–30. 59. Tolwani AJ, Campbell RC, Stofan BS, Lai KR, Oster RA, Wille KM. Standard versus high-dose CVVHDF for ICU-related acute renal failure. J Am Soc Nephrol. 2008;19(6):1233–1238. 60. Schiffl H, Lang SM, Fischer R. Daily hemodialysis and the outcome of acute renal failure. N Engl J Med. 2002;346(5):305–310. 61. VA/NIH Acute Renal Failure Trial Network, Palevsky PM, Zhang JH, O’Connor TZ, et al. Intensity of renal support in critically ill patients with acute kidney injury. N Engl J Med. 2008;359(1):7–20. 62. Palevsky PM, Liu KD, Brophy PD, et al. KDOQI US commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. Am J Kidney Dis. 2013;61(5):649–672. 63. James M, Bouchard J, Ho J, et al. Canadian society of nephrology commentary on the 2012 KDIGO clinical practice guideline for acute kidney injury. Am J Kidney Dis. 2013;61(5):673–685.
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